Open AccessLipooligosaccharide and Polysaccharide Capsule: Virulence Factors ofNeisseria meningitidisThat Determine Meningococcal Interaction with Human Dendritic Cells
Author(s) -
Alexandra Unkmeir,
Ulrike Kämmerer,
Anne Stade,
Claudia Hübner,
Sabine Haller,
Annette KolbMäurer,
Matthias Frosch,
Guido Dietrich
Publication year - 2002
Publication title -
infection and immunity
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.508
H-Index - 220
eISSN - 1070-6313
pISSN - 0019-9567
DOI - 10.1128/iai.70.5.2454-2462.2002
Subject(s) - neisseria meningitidis , microbiology and biotechnology , proinflammatory cytokine , biology , chemokine , phagocytosis , virulence , virulence factor , secretion , tumor necrosis factor alpha , neisseriaceae , virology , immune system , immunology , inflammation , bacteria , antibiotics , gene , biochemistry , genetics
In this work we analyzed the roles of meningococcal lipooligosaccharide (LOS) and capsule expression in the interaction of Neisseria meningitidis with human dendritic cells (DC). Infection of DC with serogroup B wild-type meningococci induced a strong burst of the proinflammatory cytokines and chemokines tumor necrosis factor alpha, interleukin-6 (IL-6), and IL-8. In contrast, a serogroup B mutant strain lacking LOS expression barely led to cytokine induction, demonstrating that meningococcal LOS is the main mediator of the proinflammatory response in human DC. Sialylation of meningococcal LOS did not influence cytokine secretion by DC. However, we found the phagocytosis of N. meningitidis by human DC to be inhibited by LOS sialylation. In addition, the expression of the meningococcal serogroup A, B, and C capsules dramatically reduced DC adherence of N. meningitidis and phagocytosis to some extent. Hence, LOS sialylation and capsule expression are independent mechanisms protecting N. meningitidis from the phagocytic activity of human DC.